EphA4 is a member of the receptor tyrosine kinase family. Ephrin type A and type B are known as ligands of EphA4. Upon binding of EphA4 to its ligand ephrin, deadhesion signals are induced. EphA4 is expressed in motor neurons and regulates correct axonal guidance through ephrin expressed in non-projective regions of the motor neurons in the spinal cord during a neural network formation stage.
Previous studies suggest that the functional inhibition of EphA4 is an effective therapeutic procedure for neurodegenerative diseases such as amyotrophic lateral sclerosis (hereinafter, also referred to as “ALS”) and Alzheimer's disease, and spinal cord injury.
The EphA4 gene has been reported to adjust the phenotype of ALS (Patent Literature 1; and Non-Patent Literature 1). Genetic defect of EphA4 or antagonism by EphA4-Fc or the like has been found to promote axonal elongation or functional recovery at the time of spinal cord injury in mice or rats (Non-Patent Literature 2; and Non-Patent Literature 3).
KYL peptide and compound 1 are known as existing EphA4 signaling inhibitors (Patent Literature 1; Non-Patent Literature 1; and Non-Patent Literature 2). However, there has been no report on an antibody having neutralizing activity.